Expression of parotid secretory protein (psp) in murine lacrimal
glands and its possible function as a bacterial binding protein in
exocrine secretions.
Robinson, Christopher P., Denise E. Bounous, Connie E. Alford, Kim-Hoa
T. Nguyen, Joy M. Nanni, Ammon B. Peck, and Michael G. Humphreys
-Beher.
Department of Pathology and Laboratory Medicine & Department of
Oral Biology, University of Florida, Gainesville, Florida, USA,
Department of Pathology, College of Veterinary Medicine, University
of Georgia, Athens, Georgia, USA
APStracts 3:0249G, 1996.
Non-obese diabetic (NOD) mice, an animal model for Type I autoimmune
diabetes and autoimmune sialoadenitis, abnormally express parotid
secretory protein (PSP) in the submandibular glands (Robinson, et al,
Clinical Immunol. Immunopathol. 79: 50-59, 1996). To evaluate
possible PSP gene dysregulation in the NOD mouse, we have examined a
number of organs and tissues for PSP mRNA transcripts and protein
expression. Results indicate that PSP is produced in the lacrimal
glands of NOD mice as well as most laboratory mouse strains. While
purified salivary PSP from C3H/HeJ or BALB/c mice fail to affect
amylase enzyme activity in in vitro assays, PSP bound to whole
bacteria in a Zn2+-dependent manner. Additionally, radiolabeled
protein bound to specific bacterial membrane proteins using a ligand
binding assay. PSP gene transcription, but not protein production,
was observed in the heart and pancreas from NOD mice, indicating
abnormal transcription of the PSP gene. Sequence analysis of PSP cDNA
from NOD mice revealed numerous base differences (compared to the
published PSP sequence) capable of leading to significant amino acid
substitutions, suggestive of strain specific differences for the
protein in mice. Together these results suggest that there exists in
the NOD mouse a dysregulation of PSP transcription in various
tissues. However, except for C3H/HeJ mice, PSP appears as a normal
product of the lacrimal glands where, as in saliva, it may function
as a non-immune anti-microbial agent in the protection of tissue
surfaces exposed to the external environment.
Received 11 June 1996; accepted in final form 9 October 1996.
APS Manuscript Number G235-6.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996